Research Advances in Mitophagy in Hepatic Ischemia-Reperfusion Injury

Hepatic ischemia-reperfusion injury (IRI) is a prevalent pathophysiological phenomenon encountered during liver surgeries and transplantation, leading to hepatocyte damage and liver dysfunction, which significantly affects patient prognosis. In recent years, the role of mitophagy in hepatic IRI has garnered considerable attention. Mitochondria, known as the "powerhouses" of the cell, are crucial for maintaining normal cellular physiological functions. During the ischemia-reperfusion process, mitochondria are susceptible to damage, generating excessive harmful substances, such as reactive oxygen species (ROS), which further exacerbate cellular injury. Mitophagy is a selective cellular self-protection mechanism that maintains the quality and quantity balance of mitochondria within cells by clearing damaged or dysfunctional mitochondria. In the context of liver IRI, the activation of mitophagy is of significant importance. On one hand, mitophagy can rapidly remove damaged mitochondria, thereby reducing the release of harmful products and alleviating oxidative stress and cellular damage. Research has indicated that under ischemia-reperfusion conditions, mitophagy-related pathways are activated, promoting the clearance of damaged mitochondria. On the other hand, mitophagy also regulates cellular energy metabolism, providing essential energy support for cells under stress. With the continuous advancement of research, the understanding of the role of mitophagy in hepatic IRI has become increasingly clear. Numerous studies are dedicated to exploring the specific molecular mechanisms of mitophagy and its regulation, aiming to develop new therapeutic strategies to alleviate hepatic IRI. Although studies have demonstrated that mitophagy has a protective effect in hepatic ischemia-reperfusion injury, many issues still require further investigation. First, it is essential to further elucidate the mechanisms underlying the role of mitophagy in ischemia-reperfusion. Additionally, understanding how to mitigate liver ischemia-reperfusion injury through the modulation of mitophagy represents a key focus for future research. Future studies may encompass drug development, gene therapy, and cell therapy approaches aimed at improving the prognosis of patients affected by liver ischemia-reperfusion.